Spectrum of potentially lethal cardiac conditions presenting with fetal sinus bradycardia: a report on 34 cases
A. Nair, V. Doughty, L. Vazquez‐Garcia, J. Till, J. S. CarvalhoABSTRACT
Objective
Fetal sinus bradycardia (FSB) is usually a benign antenatal finding but it can be a marker of an underlying serious condition that manifests in later life. The aim of this study was to report the antenatal course and postnatal outcome of FSB.
Method
This study was a retrospective review of all cases of persistent FSB, defined as a fetal heart rate (FHR) < 3 rd percentile for gestational age (GA) with 1:1 atrioventricular conduction on at least two consecutive fetal echocardiograms, diagnosed between January 2014 and December 2024 at the Brompton Centre for Fetal Cardiology, London, UK. Cases of isomerism were excluded, but fetuses with congenital heart disease (CHD) and normal situs were included. Antenatal data retrieved included GA at diagnosis, indication for referral, family history of any CHD or inherited arrythmia, maternal history of medication or medical conditions, fetal echocardiographic findings and sequential FHR measurements. Postnatal data included the results of 12‐lead electrocardiography, echocardiography, 24‐h Holter monitoring, genetic testing and final diagnosis.
Results
The final cohort comprised 34 cases with persistent FSB, resulting in 33 live births and one termination of pregnancy for multiple extracardiac anomalies. Indications for referral included fetal bradycardia ( n = 20), suspected CHD ( n = 5), maternal anti‐Ro antibodies ( n = 1) and a family history of long QT syndrome (LQTS) ( n = 5), cardiomyopathy ( n = 2) or CHD ( n = 1). Associated structural cardiac abnormalities were present in seven fetuses, including biventricular hypertrophy related to hypothyroidism ( n = 2), hypertrophic cardiomyopathy ( n = 1), hypoplastic left heart syndrome( n = 1), bilateral superior vena cava ( n = 1), left ventricular non‐compaction (LVNC) ( n = 1) and a small ventricular septal defect ( n = 1). Postnatal diagnoses included LQTS ( n = 10), sinus‐node dysfunction (SND) ( n = 6), LVNC ( n = 2), Albright's hereditary osteodystrophy with hypothyroidism ( n = 2), histiocytoid cardiomyopathy ( n = 1), catecholaminergic polymorphic ventricular tachycardia ( n = 1) and myotonic muscular dystrophy ( n = 1). The remaining 11 cases were classified as ‘normal’. Genetic reports were available in 22 patients, of whom seven had mutations in KCNQ1 , three in KCNH2 , two in GNAS1 and one each in NDUFB11 , RYR2 , CDH7 and DMPK ; one patient had a variant of unknown significance and five had normal results. Cascade testing detected affected family members in 2/4 de‐novo cases of LQTS and in the one case of catecholaminergic polymorphic ventricular tachycardia. Only one neonate, who had SND (anti‐Ro related), required a pacemaker at 4 years of age.
Conclusion
FSB could be the first manifestation of serious underlying cardiac conditions, including inherited arrhythmia syndromes, cardiomyopathy and SND, and needs careful antenatal and postnatal evaluation. Cascade testing allows the identification of potentially at‐risk first‐degree relatives, thereby enabling prompt intervention and appropriate management. © 2026 International Society of Ultrasound in Obstetrics and Gynecology.